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Ation ?genetics ?prenatal environment ?transcriptomeDennis R Grayson1 Alessandro Guidotti*,1 Department of Psychiatry, The Psychiatric Institute, University of Illinois at Chicago, 1601 W. Taylor St., Chicago, IL 60607, USA *Author for correspondence: Tel.: +1 312 413 4577 dgrayson@ psych.uic.eduThe Center for Disease Control estimates that approximately one in 88 children are diagnosed with au
Cent findings, additional work is now needed to further our understanding of the underlying biology of how various risk genes interact and the role of the environment in shaping these interactions. In spite of the recent identification of large numbers of ASD risk genes and associated pathways, current estimates indicate that syndromic ASD accounts for less than 10 of total diagnoses [15] . Curr
The observation that 70 of children diagnosed with idiopathic ASD exhibit comorbid medical, developmental or psychiatric conditions [3,6] , including intellectual disability [7] . According to one review, over 100 genes have been linked to syndromic forms of autism [8] . In addition, therepart of10.2217/epi.15.92 ?Dennis R GraysonEpigenomics (2016) 8(1), 85?ISSN 1750-PerspectiveGrayson Guidott
S, it seems plausible that the ultimate impact of genetic mutation lies in the downstream consequences of altered gene expression and function. The goal for the foreseeable future is to provide a better understanding of how specific genes function to disrupt specific biological pathways and whether these pathways are amenable to pharmacotherapeutic interventions.Epigenomics (2016) 8(1)future scie
Cent findings, additional work is now needed to further our understanding of the underlying biology of how various risk genes interact and the role of the environment in shaping these interactions. In spite of the recent identification of large numbers of ASD risk genes and associated pathways, current estimates indicate that syndromic ASD accounts for less than 10 of total diagnoses [15] . Curr
This proportionality [40] . These data support the idea that CpG and CpH methylation are independently regulated. DNA methylation is initiated and maintained by members of the DNMT family (DNMT1, DNMT3A, DNMT3B and DNMT3L) of DNA writers which methylate cytosine to form 5-methylcytosine (5mC) (see Figure 1). DNMT1 is involved in maintaining the methylation status of CpGs during replication and is
Ble for the disrupted neuronal/synaptic function observed in ASD [26] . A recent transcriptome analysis of multiple ASD brain regions confirms these findings and also implicates genes associated with the activation of microglia and the immune response [20] . The microglial cell state module, which negatively correlates with the synaptic transmission module, includes genes associated with the type
On of cytosine using S-adenosyl methionine and DNA as substrates. DNA methylation is a stable epigenetic mark that when located proximal to regulatory elements associated with transcription start sites, including promoters, most often facilitates the formation of a repressed chromatin state (reviewed in [33,34]). Approximately 70 of CpGs genome-wide are symmetrically methylated [35] . Regions of
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